Biology subjects

Monsalve, M.

Publications and source records attributed to Monsalve, M..

3 recordsLinked to original sources

bioRxiv2025

Alkalinized Filtered Water Induces Changes in the Gut Microbiome in Inflammatory Bowel Disease.

ObjectiveThis study evaluated the effects of filtered, alkalinized water on inflammation and intestinal dysbiosis in individuals with inflammatory bowel disease (IBD). MethodsWe conducted a three-month, two-arm, randomized intervention study involving 46 patients with IBD in remission. Participants were divided into two groups: one consumed filtered water from an active filtering device, and the control group consumed water from a mock device. Blood and stool samples were collected before and after the intervention. We assessed antioxidant capacity and circulating cytokine levels from plasma. Gene expression levels of inflammatory mediators were determined using mRNA from peripheral blood mononuclear cells (PBMCs). The microbial composition of fecal samples was characterized by qPCR analysis using primers targeting 16S rRNA genes. ResultsConsumption of alkalinized filtered water significantly reduced IL1B gene expression in PBMCs. Furthermore, subjects drinking alkalinized filtered water exhibited a consistent, albeit not statistically significant, decrease in circulating IL-1{beta} and significantly lower levels of IL-4 than controls. Microbiome analysis revealed that the levels of the Bacteroides fragilis Group were significantly lower in subjects consuming tap water than in those consuming filtered water. ConclusionThese changes suggest that consuming alkalinized water for three months leads to an improved inflammatory status compared with consuming tap water.

pathology↗

bioRxiv2024

Differential effects of diphenyl diselenide (PhSe)2 on mitochondria-related pathways depending on the cellular energy status in Bovine Vascular Endothelial Cells

Cellular energy metabolism varies depending on tissue and cell type, as well as the availability of energy substrates and energy demands. We recently investigated the variations in cellular metabolism and antioxidant responses in primary bovine vascular endothelial cells (BAECs) under different energetic substrate conditions in vitro, specifically glucose or galactose. In this context, pharmacological agents may affect cells differently depending on their energy metabolism status. In this study, we aimed to characterize the effects of diphenyl diselenide ((PhSe)2), a redox-active molecule known for its prominent cardiovascular effects, on redox-bioenergetic cellular pathways under glycolytic or oxidative conditions in BAECs. Under glucose conditions, (PhSe)2 positively impacted mitochondrial oxidative capacity, as assessed by respirometry, and was associated with changes in mitochondrial cellular dynamics. However, these changes were not observed in cells cultured with galactose. Although (PhSe)2 induced the nuclear translocation of the redox sensitive nuclear factor erythroid 2-related factor 2 (Nrf2) in both glucose and galactose media, Nrf2 remained in the nuclei of cells cultured in galactose for a longer duration. Additionally, activation of another redox sensitive transcription factor, forkhead O3 (FOXO3a) was only detected in galactose media. Notably, (PhSe)2 induced the expression of genes controlling mitochondrial antioxidant capacity and glutathione synthesis and recycling in glucose media, whereas its effects in galactose media were primarily focused on glutathione homeostasis. In conclusion, our findings underscore the critical influence of cellular metabolic status on the antioxidant capacity of redox-active molecules such as (PhSe)2.

biochemistry↗

bioRxiv2019

MiR-9-5p protects from kidney fibrosis by metabolic reprogramming

MicroRNAs (miRNAs) regulate gene expression post-transcriptionally and control biological processes, including fibrogenesis. Kidney fibrosis remains a clinical challenge and miRNAs may represent a valid therapeutic avenue. We show that miR-9-5p protected from renal fibrosis in the mouse model of unilateral ureteral obstruction (UUO). This was reflected in reduced expression of pro-fibrotic markers, decreased number of infiltrating monocytes/macrophages and diminished tubular epithelial cell injury and transforming growth factor-beta 1 (TGF-{beta}1)-dependent de-differentiation in human kidney proximal tubular (HKC-8) cells. RNA sequencing (RNA-Seq) studies in the UUO model revealed that this protection was mediated by a global shift in the expression profile of genes related to key metabolic pathways, including mitochondrial dysfunction, oxidative phosphorylation (OXPHOS), fatty acid oxidation (FAO) and glycolysis, preventing their UUO-dependent down-regulation. This effect was mirrored by a prevention in the TGF-{beta}1-induced bioenergetics changes in HKC-8 cells. The expression of the FAO-related axis peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1)-peroxisome proliferator-activated receptor alpha (PPAR) was reduced by UUO, although preserved by the administration of miR-9-5p. We found that in mice null for the mitochondrial master regulator PGC-1, miR-9-5p was unable to promote a protective effect in the UUO model. We propose that miR-9-5p elicits a protective response to chronic kidney injury and renal fibrosis by inducing reprogramming of the metabolic derangement and mitochondrial dysfunction affecting tubular epithelial cells.

molecular biology↗